Anxiety and Stress Disorders (Lecture 11) Flashcards Preview

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Flashcards in Anxiety and Stress Disorders (Lecture 11) Deck (57):
1

stressor

-anything that disrupts physiological balance
-psychological or physical

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stress response

-body's adaptations designed to reestablish balance in homeostasis

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stress

-general state of stressors that provoke a stress response

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What triggers the stress response?

-perception of a stressor

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Stress response

-sympathetic nervous system response
-hypothalamic pituitary adrena (HPA) axis
-both systems send messages to the adrenal glands which release stress horomones into the bloodstream

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stress horomones (2)

-glucocoricoids
-epinephrine

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adrenal glands

-release stress hormones (glucocorticoids(cortisol)) and epinephrine (adrenaline)

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two physiological responses to stressors

1. sympatheitc nervous system (ANS)
2. hypothalamic-pituitary-adrenal axis (HPA)

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Sympathetic nervous system

-epinephrine (adrenaline) from adrenal medulla

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hypothalamic-pituitary adrenal axis

-HPA
-on in minutes (more delayed release of hormones than ANS)
-releases glucocorticoids from adrenal cortex

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Stress Response 2 components

-autonomic nervous system (works in seconds) via hormones in bloodstream
-hypothalamus pituitary adrenal axis (HPA) (works in minutes) via neurotransmitters in synaptic gap

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ANS pathway

-body realizes it is in fight or slight
-stimulates epinephrine release from adrenal medulla (immediate but not long lasting energy used)
-parasympathetic activated in order to relax(this system stores energy)

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Adrenal medulla

releases epinephrine into circulation (activated sychronously with rest of synpathetic ANS
-epinephrine can not pass throught blood brain barrier

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No parasympathetic innervation in.......

adrenals

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Effects of epinephrine

-increase in O2 via increase in heart rate, respiration, etc
-increase in glucose in blood via breakdown of glycogen in liver
-does not cross blood brain barrier
-more energy for muscle contraction
-frees up long term stored energy into usable show term energy
-blood does not travel to irrelevant areas such as sexual organs or digestive tract

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No matter what the stressor

-the response is the same

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Hypothalamus Pituitary adrenal axis (HPA)

-slower onset of effects (minutes)
-leads to the 4 F's (feeding fighting fleeing fornicating)

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hypothalamus

-makes up less than 1% of brain
-gets responses from mucles and intergrates them
-mediated feeding, flight or fight, sex
-first step in command system that deals with an imbalance in homeostasis
-direct connection to the pituitary via a blood portal system (to anterior pituitary) or neurons (posterior pituitary)

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What regulates many peripheral glands of the endocrine system? (not just the adrenals)

1. hypothalamus
2. pituitary

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Anterior pituitary

-cell bodies in PVN of the hypothalamus send axons to hypothalamo-pituitary portal system

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posterior Pituitary

-activated directly
-releases oxytocin and vapopressin
-cell bodies in paraventicular nucleur (PVN of the hypothalamus send axons to the posterior pituitary
-axon terminals release hormones into blood vessels

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oxytocin

(released by posterior pituitary)
-labor
-lactation
-pair bonding

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vasopressin

(released by posterior pituitary)
-antidiuretic
-blood pressure

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portal system

veins that carry hormones to anterior pituitary

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anterior pituitary cells

-respond to hormones and release other hormones in general circulation
-axons only go to top of portal system
-hormones take message from there
-tropic hormones

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Normal Stress response (HPA axis)

-brain relizes stressor
-hypolalamus releases corticotropin releasing hormone
-goes into blood portal system to anterior pituitary
Adrenocoticotropic hormones does to adrenal cortex
-adrenal cortex releases cortisol which gives negative feedback

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Epinephrine

works to provide short term energy resouces (glucose)
-in the liver = breakdown of glycogen to glucose

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glucocorticoids

-work to provide prolonged energy resources (glucose) from long term energy store to provide sustainable energy to prolonged stressors
-in liver = breakdown of protein and fatty acids into glucose (gluconeogenesis)
-in muscles = prtein breakdown into glucose (proteolysis)
-in adipose tissue (fat) = breakdown of fatty acids into glucose

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glucocorticoids - cortisol

-baseline cortisol release has a circadian rhythn that peaks at waking
-cortisol is also relased during copulation, excursive, drug use
-glucorticoids are released when your metabolism needs a boost

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brain regulation of sress response

-corticotropin releasing hormone (CRH) neurons of the PVN regulated by:
-the amygdala
-the hippocampus

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regualtions of sress response in the amygdala

-basal lateral nuclei is the most important
-sensory information enters basolateral amygdala (BLA)
-BLA--> central mucleus of the amygdala (CeA)
-CeA---> hypothalamus ---> stress response

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stimulation of amygdala in humans

-stress and fear
-increase CRH release

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regulation of stress response (hippocampus)

-hippocampus contain glucocorticoid receptors
-detects circulating cortisol and sends negative feedback to hypothalamus
-activation leas to decrease CRH release

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hippocampus and chronic stress

-due to extended exposure to cortisol
-reduces dendritic arbors of hippocampul neurons
-chronic stress also reduces hippocampal cell numbers
-cell death
-reduced birth of new neurons (neurogenesis)
= reduced overall hippocampus size- degeneration starts a vicious sycle in which the stress response is less regulated which results in more corisol release and more hippocampal damage

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hippocampus integral

-in learning ad memory
-vietnam combat vetrans and civtims of child abuse = reduced hippocampal volume and short-term deficits

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rats placed in present of cat for 75 minutes ---->

-infered animals ability to learn spatial task
-molecular mechanisms of learning impaired in hippocampus
-acute stress also impairs long term survival of NEW hippocampal neurons

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Psychoneuroimmunology

study of the interactioins between the immune system and behavior (e.g. the stress response)
--immune system weakened/would heal slower in those who have chronic stress

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cell mediated immunity

-antigen engulfed by macrophace
-t cell recognizes activated macrophage
-bound t cells proliferate and develop into a form that kills body cells that have been infected by the micoorganism

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antibody mediated immunity

-foreign antigen are bound by B cells with appopriate receptor

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Chonic stress diminishes immune response

-stops the maturation of lymphocytes (t cells and B cells)
- destruction of lymphocytes

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Reasoning for chronis stress diminishing immune response

-originally believed to conserve energy for the fight or flisht response
-in reality

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acute stress (5-100 minutes)

-actually enhances many elements of the immune response
-increase in number of lymphocytes in peripheral blood
increase in amount of antibodies in saliva

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glucocoticoids depress immune response by....

-released during prolonged stress are imunnosupressive to regulate

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chronic stress

-maintenance of high glucocorticoid levels during chronic stress prolongs suppression of immune system and results in below baseline immunity

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acute v chronic stress

-acute stress improves performance
-persisting stress can make us more susceptible to things because it weakens the immune system

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Anxiety disorders

-characterized by inappropriate (pathological) expression of fear
-15 percent of american will suffer from one this year
-most connon of psychiatric disorders
-GAD, SAD
-OCS
PTSD

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Panic disorder

-episodic attacks of acute anxiety causing unremitting terror (panic attacks)
-2% of population
-2x more women

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Generalized Anxiety order (GAD)

-excessive worry and anxiety for at least 6 months that prevents living "full" life
-3% of population
-2x more women

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social anxiety order (SAD)

-excessive fear of being exposed to the scrutiny of others
-leads to pathological avoidance
-5% of population
-equal in women and men

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Panic DIsorder, GAD, SAD trends

-some heredity aspect (most likely to have one if parent has it)
-temporal lobe abnormalities in 40% patients with panic disorder
-over activation of amygdala----> releases excessive amount of cortisol

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Panic DIsorder, GAD, SAD treatment

-Benzodiazpines
-SSRIs

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Benzodiazpines

-bind to GABAa receptor, opening Cl- channel, causing neuronal inhibition
-high density of GABAa receptors in amygdala
-downside: highly addictive, can lead to symptoms that you were originally trying to treat
-withdrawal = increased anxiety

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SSRIs

-anxiolytic effects NOT immediate-it takes weeks
-SSRIs do increase glucocorticoid receptors in hippocampus --> enhanced negative feedback from cortisol

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OCD characteristics

-characterized by uncontrollable thoughts (obsessions) and/or the need to perform specific acts repeatedly (compulsions)
-1-2% of population
-slightly more prevalent in females

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OCD circuit in brain

orbitofrontal cortex (OFC) --> basal ganglia --> thalamus --> back to OFC

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OFC=

-orbitofrontal cortex
-recognizes situations that have personal significance and sends "worry" message to thalamus to regulate behavior

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basal ganglia role in OCD circuit

-basal ganglia works as a "brake" suppressing original "worry" signal sent by OFC
-damage to basal ganglia may impair its ability to stop the OFC from sending continual messages= obsessions which then commend the thalamus to initiate actions= compulsions